Anti-aging formula slated to begin human trials

Things like Botox, hand creams, and hair dye exist to prolong the appearance of youth - but what if it could actually be achieved at the cellular level? A collaboration of researchers from the United States and Australia might have done just that. A regular metabolic compound that has been administered to mice has been shown to not just boost muscle function, but actually reverse the affects of aging. The research was led by David Sinclair of the University of New South Wales and the results have been published in the journal Cell.

A normal part of human aging involves senescence, which is a general wearing out of the body over time. Muscles begin to lose tone and become inflamed over time, and they also can develop insulin resistance. Without being able to use insulin, the cells aren’t able to uptake the glucose needed for activity. These problems contribute to why many elderly people have trouble getting around and athletes aren’t able to sustain certain levels of activity as they age.

A regular metabolic coenzyme known as nicotinamide adenine dinucleotide (NAD+) was administered to mice in hopes that it would slow the aging of skeletal muscle. The researchers were shocked to find that it didn’t slow aging; it dramatically reversed it. In under a week, the mice who had previously been suffering from a variety of age-related impairments experienced an increase in muscle tone, as if they had been exercising and following a healthy diet. In some regards, the compound acted like the proverbial fountain of youth.

The secret to reversing aging, as it turns out, is hidden in the mitochondria. In humans and most other species, mitochondrial DNA is passed down only by the mother. These genes are responsible for becoming the cellular powerhouse and generating ATP, which cells use for energy. The team discovered that, over time, genes from the mitochondrial genome stop interacting with genes from the nuclear genome. Administering NAD+ reverses this trend and encourages communication.

NAD+ is involved in redox reactions, which regulate electron transfer in metabolic processes. As the mice grew older and less active, their levels of NAD+ had basically been cut in half. By replenishing this critical compound in the mice, their muscles had been rejuvenated. The natural process that deteriorates skeletal muscle is the same one that affects the heart.

Human trials of NAD+ treatments will begin in 2014. If the results are anything like what was experienced by the mice, it will be the equivalent of a 60 year old having the fitness of a 20 year old. However, the treatments will not be cheap. In order to gather enough patients to do the study properly, millions of dollars will need to be raised. Though there is no telling how long it will be before this treatment hits the market, Dr. Sinclair has established a company to expedite the process if and when it is granted approval.